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Foreign Animal Diseases > Foreign Animal Diseases > Flashcards

Foreign Animal Diseases Flashcards

1
Q

Inter-epidemic Maintenance: Theory 1: Transovarial transmission in Aedes

A
  • Aedes sp. infected mosquito eggs can remain dormant for years
  • Arrival of persistent rains and flooding, eclosion of mosquito eggs results in infected vectors
  • Aedes sp. feed preferentially on cattle, which are excellent RVF virus amplifiers
  • Viremic catle subsequently infect other species of mosquitoes
  • These other mosquito species infect an even broader range of vertebrates
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2
Q

RVF DDx

A
  • Bluetongue
  • Wesselsbron disease
  • Enterotoxemia of sheep
  • Ephemeral fever
  • Brucellosis
  • Vibriosis
  • Trichomonosis
  • Nairobi sheep disease
  • Heartwater
  • Peste des petits ruminants
  • Ovine enzootic abortion
  • Anthrax
  • Toxic plants
  • Bacterial septicemias-Abortogenic agents
  • Hepatotoxic agents
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3
Q

RVF Diagnostics

A
  • VI, Immunofluorescene carried out on impression smears of liver, spleen and brain
  • AGID (useful in labs without tissue-culture facilities)
  • PCR: rapid antigen detection and to detect RVF virus in mosquito pools
  • Detection of antigen in blood/tissue: immuno-diffusion, immuno-enzyme methods and immuno-staining
  • VNT (prescribed test for international trade)
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4
Q

RVF Prevention & Control (Vaccines)

A
  • Live attenuated vaccine (Better immunity - 3 years; can cause abortions and birth defects)
  • Killed vaccine (requires 2 doses and annual booster)
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5
Q

RVF Prevention and control

A
  • Vector control, restriction of movement
  • Control of animal movements
  • controls at slaughterhouses
  • disinfestation of ‘dambos’ (methoprene hormone; controlled burning)
  • draining of standing water
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6
Q

Rinderpest (general)

A
  • cattle plague or RPV
  • Found primarily in Africa and mediterranean countries
  • eradicated worldwide
  • destorys entire populations of cattle
  • leads to famine in cattle-dependent areas
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7
Q

New World Screwworm (general)

A
  • Gusanos, Mosca Verde, Gusano barrendor, Gusaneras
  • Myiasis caused by larvae of the fly Cochliomyia hominivorax (new world)
  • Obliatory parasite found only in warm areas of Americas
  • Serious public health problem in endemic areas
  • 1966: US free of Screwworm
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8
Q

New World Screwworm (Western vs Eastern hemisphere)

A

Western Hemisphere:

  • Only the New World screwworm
  • Central and South America
  • Caribbean Islands

Eastern Hemisphere

  • Only the Old World Screwworm
  • Found in remaining tropical and sub-tropical areas
  • Never established in Europe, North Africa, the Middle East or Australia
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9
Q

RVF Inter-epidemic Maintenance Theory 2: Sylvatic Cycle

A
  • RVF virus circulates in endemic manner between mosquitos and a yet unidentified vertebrate in areas of heavey vegetation (i.e. tropical, subtropical, wooded areas); e.g. case of Semliki and Knysa viruses)
  • Outbreaks occur at periphery of vegetated areas and may “jump” to other susceptible areas
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10
Q

RVF Inter-epidemic Maintenance: Translocation of RVF

A
  • Movement of viremic animals (incubating disease)
  • Movement of vectors by warm winds
  • Transport of vectors by aircraft
  • Transport of a viremic human (e.g. tourist)
  • Intentional introduction
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11
Q

RVF Clinical Signs

A
  • salivation, anorexia, weakness
  • high fever (40-42C)
  • “Abortion Storm”**
  • nasal congestion; mucopurulent nasal discharge
  • fetid and/or bloody diarrhea
  • sudden death in young animals
  • 90% of those < 7 days; 20% of those >7 days
  • sudden death in adult sheep
  • 20% post-abortion; <10% in other adult animals
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12
Q

RVF Pathology

A
  • severe hepatitis
  • “nutmeg liver” (hepatic necrosis)
  • hemorrhages in gall bladder and abomasum
  • petechiae on serosal surfaces
  • hemorrhagic enteritis
  • hemorrhages and edema in abomasum diaphargm, and gall bladder
  • multi-focal hepatic necrosis with high intesnity eosinophilic, cytoplasmic inclusion bodies
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13
Q

New World Screwworm: Agent & lifecycle

A

Cochliomyia hominivorax Cycle

  • Fly deposits eggs at wound edge
  • Larvae hatch in 12 hours and penetrate by eating the live tissue (5 days)
  • Pupae fall to the ground and fly emerges in 8 days
  • Fly is sexually active at 2 days
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14
Q

New World Screwworm: Importation Concerns

A
  • Can transmit adult screwworms to nonendemic areas

- Importation of infested animals

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15
Q

New World Screwworm: Animal Transmission

A
  • Female fly deposits eggs into wound
  • Larvae feed on living tissue
  • Multiple infestations in one wound are common
  • Non-contagious

*Hosts (all warm-blooded)

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16
Q

New World Screwworm: Human Transmission

A
  • Infected in same manner as animals

- Can transmit adult screwworms to nonendemic areas

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17
Q

New World Screwworms: Clinical Signs

A
  • Larvae visible in wound by 3 days (May be hundreds present)
  • Bloody discharge
  • Foul-smelling odor
  • depression
  • off-feed
  • separation
  • attempt to control discomfort
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18
Q

New World Screwworm: Morbidity/mortality

A

Morbidity: high, weight loss and drop in lactation
Mortality: high in untreated animals
-death can occur in 7-14 days due to toxicity, secondary infections or combo of both

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19
Q

New World Screwworm: Diagnosis

A
  • Suspect in any animal with draining and enlarging wounds
  • differentials include any fly larvae that infest wounds (several types may be present)
  • samples to collect (larvae from the deepest portion of the wound)
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20
Q

New World Screwworm: Treatment

A
  • Obtain samples first
  • Topical application of larvicide (2-3 successive days)
  • Spray or dip with organophosphate - Prevents reinfestation
  • Treatment of human cases
    • Removal of larvae, debridement, if necessary, good hygiene
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21
Q

New World Screwworm: Prevention and Control

A
  • Notify autorities, treat infested wounds with larvicide and suspend animal movement
  • Eradication: very succesful by use of sterile male flies; southern US and Central America are now free
  • Screwworm flies mate once in a lifetime, and if one of the insect pair has been sterilized with gamma rays, neither will reproduce
  • surveillance in nonendemic areas (prevent importation)
  • frequent animal inspections in endemic areas (organophosphate treatment)
  • seasonal avoidance
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22
Q

Sheep & Goat Pox: Agent

A

-Family: Poxiviridae (Genus: Capripox)
-Sheep Pox VIrus (SPV) & Goat Pox Virus (GPV) are genetically distinct with strong host preference
~Some isolates can cause disease in both sheep and goats
~Recombination of the two occurs with mixed host preference

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23
Q

Sheep & Goat Pox: Hosts

A

-Sheep and Goats
~European sheep breeds highly susceptible
~Not seen in wild ungulates
-No conclusive evidence of infection in humans
-Anecdotal reports of sheep or goat pox lesions in humans in Indian and Sweden
~Not verified by virus isolation

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24
Q

Sheep & Goat Pox: Transmission

A
  • Infectious virus present in all secretions, excretions and scabs
  • Direct contact (skin abrasions and mucous membranes)
  • Aerosols (inhalation)
  • Vectors (Fomites and biting insects - mechanical vector)
  • Carriers (subclinical cases)
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25
Q

Sheep & Goat Pox: Clinical Signs

A

Fever, conjunctivitis, depression, anorexia, dyspnea, nasal or ocular discharge, secondary bacterial infections are common

  • Looks like ORF but all over body
  • papules forming into hard scabs
  • lesions may cover body or be restricted to **axilla, perineum and groin, ears or tail **
  • Death may occur at any stage
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26
Q

Sheep & Goat pox: Incubation, morbidity/mortality

A

Incubation Period: 4-13 days
Morbidity: up to 80%
Mortality: 50-90% (higher in young)

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27
Q

Sheep & Goat Pox: DDx

A 
contagious exthyma
bluetongue
mycotic dermatitis
sheep scab
mange
photosensitization
peste des petits ruminants
parasitic pneumonia
caseous lymphadenitis
insect bites
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28
Q

Sheep & Goat pox: diagnosis

A

Clinical:
-suspect in febrile animals with characteristic full-thickness skin lesions

Laboratory:

  • Do not sample scabs
  • Viral isolation, electron microscopy
  • Numerous antigen tests
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29
Q

Sheep & Goat Pox: Prevention & Control Endemic Areas

A

-Vaccinate

Outbreak in endemic area - small scale

  • Quarantine, slaughter infected and exposed, clean and disinfect
  • ring vaccination

Outbreak in endemic area - large scale

  • Massive vaccination
  • movement restrictions
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30
Q

Sheep & Goat Pox: Prevention and Control Non-endemic Areas

A

-keep free with import restrictions and proper quarantine
-Prevent introduction of infected animal products
~Meat, hair, wool, hides
~Virus found on wool or hair for 3 months after inoculation

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31
Q

Sheep & Goat Pox: Prevention and Control - Outbreak in Non-endemic areas

A
  • Quarantine, slaughter infected and exposed, clean and disinfect
  • ring vaccination
  • No carrier state
  • Isolate infected herds and sick animals for at least 45 days after recovery
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32
Q

Sheep & Goat Pox: Prevention and Control: Disinfection

A
  • sodium hypochlorite
  • phenol 2% for 15 minutes
  • Detergents

-**Virus can survive:
~6 months in the environment
~2 months in wool
~Extended periods in dried scabs

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33
Q

Vesicular DIseases

A
  • Viral diseases
  • Mainfested by lameness, vesicular lesions and subsequently erosions of epithelium of mouth, nares, muzzle, feet and teats
  • Vesicular diseases are clinically indistinguishable from each other. Laboratory confirmation is required.
  • Foot and Mouth Disease (FMD); Vesicular Stomatitis (VS); Swine Vesicular Disease (SVD); Vesicular Exanthema of Swine (VES);

*Seneca Valley Virus, or Seneca Virus A (SVA) is an endemic FMD look alike-outbreaks in swine herds in the midwest and southeast in 2015

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34
Q

Foot and Mouth Disease: Agent

A

Picornaviridae, Apthovirus

Virus Serotypes: 7 types (with >60 immunological different subtypes)

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35
Q

FMDV Stability

A
  • highly sensitive: pH <6 or >9
  • somewhat sensitive; UV sunlight
  • inactivated at >70C (158F)/30 minutes
  • sensitive; many disinfectants
  • sensitive: dry environment
  • Stable: in moist, organic-rich materials
  • stable: low temperatures
  • survives regular milk pasteurization
  • inactivated by ultra heat treatment (UHT) pasteurization
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36
Q

FMD and public health

A
  • FMD is not considered a zoonotic disease
  • humans are not clinically susceptible to FMDV (few lab-related infections reported)
  • **not to be confused with “hand-foot-mouth disease” caused by human coxsackie A6 virus and other enteroviruses (same virus family - picornaviridae)
  • However, FMD does cause a negative impact on public health (mental health - increased rate of suicides; affects nutrition by decreases in the availability of animal protein)
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37
Q

FMD Transmission

A
  • FMD found in all excretions and secretions including expired air
  • Inhalation of aerosols
  • Direct contact
  • Ingestion, meat products (except deboned, aged (pH <5.7)
  • Fomites
  • Carrier state
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38
Q

FMD Incubation/Duration/Morbidity

A

Incubation: 2-14 days (14 days by OIE terrestrial animal health code)

Duration: 1-3 weeks

Morbidity: Extremely high (approx 100%)
Adult CFR: 1-5%
Young CFR: 20% or higher
*necrotizing myocarditis
Carriers: Yes, in ruminants
Cattle - not shedders
African buffalo - shedders
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39
Q

FMD Humans as hosts

A

-very rarely develop mild clinical signs
-may carry in nasal passages
~some discrepancy in reports and recommendations based on risk of transmission
~48 hr avoidance of susceptible animals
~Extended avoidance not needed if good biosecurity and hygiene are followed

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40
Q

FMD Hosts: Sheep & Goats

A

Maintenance hosts

Carriers: pharyngeal tissue 4 - 6 months

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41
Q

FMD Hosts: Pigs

A

Amplifier host

No carriers

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42
Q

FMD Hosts: Catle

A

Indicator/Sentinel Hosts

Carrier: pharyneal tissue 4 - 6 months

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43
Q

FMD Clniical signs

A

-Fever and vesicles (feet, mouth, nares, muzzle, teats)
~progress to erosions

  • Abortion
  • Death in young animals
  • Recover in 2 weeks unless secondary infections arise
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44
Q

FMD Clinical signs: cattle

A

Oral Lesions (+ drooling)

Teat lesions

Hoof lesions (interdigital space, coronary band, lameness)

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45
Q

FMD Clinical signs: pigs

A

Hoof lesions (more severe than cattle)

Snout vesicles

Oral vesicles less common (drooling is rare)

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46
Q

FMD clinical signs: Sheep & Goat

A
  • mild, if any, signs (fever, oral lesions, lameness)

- makes diagnosis and prevention of spread difficult

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47
Q

FMD Pathology

A

-Clinically indistinguishable from other vesicular diseases, especially swine
-single or multiple vesicles
-various stages of development
~white area, 2mm-10cm
~Fluid filled blisters
~red erosion, fibrin coating
-dry lesions
-tiger heart - myocardial necrosis

*Only FMD causes lesions of the rumen pillars

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48
Q

FMD Diagnosis

A

-Notify authorities and wait for instructions before collecting samples
-Vesicular fluid & vesicular epithelium
~Virus isolation; ELISA for antigen, CF for antigen, rRT-PCR tests
-Nasal swabs (rRT-PCR test)
-Serum (acute & convalescent)
~ ab titers

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49
Q

FMD Prevention and control

A

-**USDA-APHIS: STRICT IMPORT RESTRICTIONS
~prohibit live ruminants, swine, and their products from FMD-affected countries
~Monitor travelers and belongings at ports of entry

  • State planning/training exercises
  • Biosecurity protocols for livestock facilities
  • Decontamination and disposal of foreign garbage
  • Strong animal health infrastructure
  • Reportable disease - prompt diagnosis
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50
Q

FMD Control & Eradication

A
  • Quarantine
  • Stop movement of animals and products
  • Rodent Control
  • Cleaning and Disinfection
  • Disinfection of vehicles and personnel
  • Slaughter of infected and contact animals
  • Destruction of infection carcasses (incineration, rendering, burial)
  • Strategic vaccination

*areas must be free of organic matter

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51
Q

FMD Control & Eradication: Disinfection

A 
Effective solutions include:
2% sodium hydroxide (lye)
4% sodium carbonate (soda ash)
5.25% sodium hypochlorite (household bleach)
0.2% citric acid
Virkon-S
52
Q

FMD Vaccination

A
  • killed vaccine, serotype and strain specific
  • North American Foot-and-Mouth Vaccine Bank (Plum Island, NY)
  • Monitor disease outbreaks worldwide and stock active serotypes and strains
  • It is essential to isolate virus and identify the serotype to select the correct vaccine
53
Q

FMD Vaccination - in the US

A

-US has no need to vaccinate (have not had animals affected since 1929)
-May be used to control an outbreak
-Huge implications if we do vaccinate
~Annual re-vaccination required
~Costly, time consuming
~Does not protect against infection, just clinical signs
~Spread infection to other animals
~International trade status harmed

54
Q

Vesicular Stomatitis

A
  • Viral Disease of horses, cattle, and swine
  • Outbreaks are more common near Equator
  • OIE reportable disease (trade barrier)
  • Unlike FMD, VS occurs sporadically in the US
  • costly, >14M in 1995
  • little known abbout epidemiology and natural cycle
  • mechanisms of disease and protection against disease remain unclear
55
Q

VSV: Agent

A

RNA visculovirus
Family: Rhabdoviridae
2 major serotypes: Indiana & New Jersey

4 viruses cause VS
~VSV-IN; VSV-NJ; Cocal; VSV-AV

56
Q

VSV: Hosts

A
  • Affects horses, cattle, swine, camelids, and humans
  • Sheep and goats occasionally
  • Note: llamas get VS, not FMD
57
Q

VSV Transmission in animals

A 
-Vectors
  ~**Sandflies**
  ~**Blackflies**
  ~**mosquitoes**
  ~Seasonal outbreaks - starts in warm area &amp; moves to cooler area via vectors

-Direct Contact
~Infected animals
~Contaminated objects

58
Q

VSV Transmission - humans

A 
-Vectors
   ~Sandflies
   ~Blackflies
   ~Seasonal outbreaks
-Direct Contact
    ~Infected animals
    ~Contaminated objects
-Contact with infected tissues, vesicular fluid, saliva
-Vector injection
    ~Blackfly, sandfly
-Aerosol transmission in a laboratory setting
59
Q

VSV Clinical signs - animals

A 
Incubation period: 2 - 8 days
Excessive salivation
Fever and vesicles that resemble FMD
-Horses severely affected
   ~oral lesions (drooling, chomping, mouth rubbing)
   ~coronary band lesions
   ~morbidity: 90% but variable
   ~mortality: low (death of young not as common as FMD)
60
Q

VSV Clinical signs - humans

A 
Incubation period: 1- 6 days
Influenza-like symptoms:
  ~headache, fever, retrobulbar pain, malaise, nausea, limb and back pain, oral vesicles (rare), photophobia
-Self-limiting disease, supportive care
-Recovery can be prolonged
-Death is rare
61
Q

VSV Pathology

A 
-Erosive, ulcerative lesions
   ~Oral cavity, teats, coronary bands
   ~***No lesions in rumen or heart***
-Histology
    ~Degeneration of epithelial cells
-Electronmicroscopy
    ~Virus in fresh lesions, vesicular fluid
62
Q

VSV Laboratory Diagnosis

A

-Viral Antigen
~From vesicular fluid or epithelium
~ELISA, complement fixation, virus neutralization
-Antibody tests
~Paired serum samples
~ELISA, complement fixation, virus neutralization

63
Q

VSV Prevention

A
  • Do not buy from positive herds for 3 months post-infection
  • Avoid grazing at peak insect feeding hours
  • Segregation and isolation necessary for controlling spread
  • Move into stables
  • Sanitation
  • Insect control programs
64
Q

VSV Control

A

Vaccines
Understanding life cycle (vector control - limit exposure)
Quarantine issues

65
Q

VSV Control - vaccines

A
  • none commercially available in the US
  • inactivated bivalent tested oil adjuvant: effective
  • Under development: live attenuated with marker
  • mechanism of protection poorly understood
66
Q

VSV Control - Quarantine issues

A
  • Requires understanding epidemiology
  • Quarantine infected facilities/animals
  • No movement of animals for at least 21 days after all lesions have healed
67
Q

VSV Disinfection

A
  • Area must be free of organic matter
  • Inactivated by sunlight
  • Active 3 - 4 d on fomites
  • contact time of at least 10 minutes
  • soda ash
  • 2% iodophore
  • chlorine dioxide
  • 1% chlorine bleach
  • 1% cresylic acid
  • Quaternary ammonium
68
Q

VSV Public Health Significance

A
  • Low incidence of human illness
  • Chance of infection when handling contaminated tissues (Biosafety level 3 / PPE)
  • Rarely causes vesicle formation
  • Recover in 4 - 7 days
69
Q

Swine vesicular Disease (SVD)

A

A contagious, viral vesicular disease of swine, characterized by fever, vesicular lesions and, subsequent erosions of the epithelium of the mouth, nares, snouth, feet and teats

70
Q

SVD Agent

A 
Family: Picornaviridae
Genus: Enterovirus
-Related to human enterovirus
-Unrelated to other porcine enteroviruses
-Survives for long periods in environment and in meat products
-resistant to:
  ~desiccation and freezing
   ~Temperatures up to 157F
   ~pH ranging from 2.5-12
71
Q

SVD Virus Stability

A

-pH stability: <2.5 or >11
-Acid stable = enterovirus
-Not inactivated by post rigor-mortis drop in muscle pH
-UV sensitive: somewhat sensitive to sunlight
-survives in moist, organic-rich materials
-remains in many meat products
-180 days to > 1 year in hams
>1 year in dry cured sausages**
>2 years in processed intestinal casings

72
Q

SVD Transmission - Animal transmission

A

-Inhalation
-Contact
~Infected animals, feces (fecal-oral), fomites (broken skin, MM)
-Ingestion
~Contaminated meat scraps
-Excretion of Virus
~Nose, mouth, feces
~Up to 48 hours before clinical signs seen
~Shed in feces for >3 months after infection

73
Q

SVD Transmission - Human transmission and clinical signs

A
  • seroconversion reported in lab workers but not vets or farmers
  • symptomatic cases have been mild with flu-like symptoms (weakness, abdominal pain, myalgia)
  • one case of meningitis
74
Q

SVD Clinical signs

A

-Incubation Period: 2-7 days
-Very similar to foot-and-mouth disease
-Vesicles and erosions
~snouth, mammary glands, coronary band, interdigital areas
-Neurological signs rare
-Abortion not typically seen
-Recovery within 2 - 3 weeks (little permanent damage)

75
Q

SVD Pathology

A

Vesicles are the only PM lesions

76
Q

SVD Prevention and Control

A

-Quarantine infected facilities/animals
-Slaughter
~infected pigs
~Pigs in contact with SVD
~Disposal
-Disinfection
~1% sodium hydroxide + detergent
~oxidizing agents
~iodophor + detergents
-Vaccination
~Never been done
~Inactivated vaccines (not commercially available)

77
Q

Vesicular Exanthema of Swine (VES)

A
  • VES is a contagious viral vesicular disease of swine, characterized by fever, vesicular lesions and, subsequent erosions of the epithelium of the mouth, nares, snout and feet
  • An indistinguishable disease of swine can be produced by infection with one of several caliciviruses isolated from seals, sea lions, and marine fish (San Miguel Sea Lion Virus)

**US declared free of VES/ VES = FAD in 1959

78
Q

Virus/Family/Genus

FMD, VS, SVD, VES

A

FMD:
F: Picornaviridae; G: Aphtovirus

VS:
F: Rhabdoviridae; G: Vesiculovirus

SVD:
F: Picornaviridae; G: Enterovirus

VES:
F: Caliciviridae; G: Vesivirus

79
Q

VES: Agent

A

Family: Caliciviridae
Genus: Vesiviridae
Serotypes: 13 types of VES virus; 12 types of San Miguel Sea Lion Virus

80
Q

VES Hosts

A
  • Swine

- Humans are NOT susceptible

81
Q

VES Transmission

A
  • Feces (fecal-oral)
  • Direct contact
  • Blood (ingestion)
  • Meat products (ingestion)
82
Q

VES Disease duration

A

Incubation: 1 - 5 days
Duration: 1 - 3 weeks

83
Q

VES Epidemiology

A

Morbidity: low to moderate
Case fatality rate: very low
Carriers: not known
Maintained as subclinical infections

84
Q

VES Clinical Signs

A
  • Fever, lameness, blanching of coronary bands, vesicles and erosions
  • Clinical signs are very similar to those of foot-and-mouth disease and other vesicular diseases. There is a fever; vesicles in the mouth, on the snouth, and on the feet and lameness.
  • These signs are all grossly indistinguishable from FMD. Lesions in VES seem to be deeper, and granulation tissue commonly forms especially on the feet
85
Q

VES Pathology

A
  • Epithelial lesions are identical to the other vesicular diseases
  • NO SYSTEMIC LESIONS
86
Q

VES Control

A

Slaughter and disposal of infected and contact animals

Disinfection of the premises

87
Q

Porcine Diarrhea Virus (PEDV)

A

PEDV new disease to the US that was confirmed on May 16, 2013 by USDA NVSL

  • Found in multiple farms simultaneously and additional farms diagnosed positive
  • Retrospective diagnosis as early as April 2013
88
Q

PEDV Clinical Signs

A

Baby piglets - dead in 5 days
growers - explosive diarrhea
sows - febrile, lethargic and scouring during late gestation or 2-3 days before farrowing

89
Q

PEDV - general

A

PEDV is a positive-sense, enveloped, single-stranded RNA virus
-Different strains of PEDV exist with virulence dependent upon the spike (S) gene sequence

90
Q

PEDV - history

A
  • in 2013, PEDV declared a “transboundary disease” by USDA and considered non-regulatory at that time but later became regulated after June 2014
  • The virus had not previously been identified in teh US
  • Genomic evaluation determined that the US PEDV strain was 99.4% similar to a Chines isolate from 2012** (strain info from Genbank)
91
Q

PEDV - transmission

A
  • PEDV = fecal/oral method of infection and transmission
  • Transmits through contaminated manure; anything in contact with manure can be a potential source of infection
  • PEDV does NOT affect pork and cannot infect humans
  • PEDV is not a public health or food safety issue
92
Q

PEDV Stability

A

PEDV can survive in many different conditions:

  • survival in pits as low 6 months after infection
  • virus can be found at 4 months postinfection
  • survive in cold conditions
  • can survive in dry and slurried feed, and in various feed ingredients
  • can survive in manure slurry, feces, water (fresh and recycled)
  • PEDV survivability can be time dependent (pit manure)
93
Q

Key biosecurity measures (PEDV)

A
  • For pit/manure management, start with farms that have most time since initial infection and work to most recently infected
  • Clean and disinfect between sites (remove organic materials)
94
Q

PEDV biosecurity - transportation management

A

Certain procedures for trucks can kill the virus:
-160F for 10 minutes kills PEDV
-68F for 7 days kills PEDV
-Clean, disinfect and heat (see above) can kill PEDV and other pathogens!
~Quaternary ammonium/gluteraldehyde
~Accel - hydrogen peroxide mix
~Others…(bleach; phenolics etc)

95
Q

Key biosecurity measures (PEDV)

A

Prevent contamination as much as possible

  • Create a “line of separation”
  • keep clean and dirty equipment separate
  • avoid contamination of high risk areas

Focus on removal of organic material for effective cleaning and disinfection

Recently infected farms = higher risk than farms with longer time after initial infection
~HIGH virus load in environment around the farm
~Biosecurity and sanitation of equipment is critical

96
Q

Avian Influenza - general

A

Family: Orthomyxoviridae
Genera: A, B, C viruses; Thogotovirus; isavirus

-negative sense RNA virus
-segmented genome
replicate in nucleus

97
Q

Influenza Virus (describe subtypes)

A
  • 16 hemagglutinin subtypes
  • 9 neuraminidase subtypes
  • 2 nonstructural subtypes
98
Q

Influenza virus - naming

A/Chicken/Pennsylvania/1370/83 (H5N2)

A 
A = antigenic type
Chicken = isolate host of origin
Pennsylvania = Geographic location
1370 = isolate reference
83 = year of isolation 
H5 = Hemagglutinin subtype
N2 = Neuraminidase subtype
99
Q

Avian Influenza - in birds and other species

A
  • Avian influenza is naturally found in wild birds and not normally found in domestic ducks, chickens and turkeys
  • Virus infection is not normally thought to cause disease in its natural host (viruses are low pathogenic)
  • Wild bird surveys have shown certain duck, gull and shorebirds species are commonly infected at different times of the year
  • *All type A influenza viruses are thought to originate from wild birds
100
Q

Highly Pathogenic Avian Influenza

A
  • Systemic, rapidly fatal disease of poultry
  • Only H5 & H7 subtypes are recognized to cause HPAI
  • OIE List A Disease - outbreaks are reportable
  • HA cleavage site critical virulence factor
  • *Low pathogenic H5 and H7 AI viruses can mutate into the highly pathogenic form of the virus
101
Q

Avian Influenza - Evolution - Antigenic Drift

A

Small changes (mutations) in genes that happen continually. Usually share antigenic properties but fi not, body immune system or vaccine may not recognize it. Vaccine cross protection becomes an issues

102
Q

Avian Influenza - Evolution - Antigenic Shift

A

Re-assortment occurs and an abrupt, major change in influenza virus occurs, resulting new hemagglutinin and/or hemagglutinin and neuaraminidase proteins - novel, pathogenic and virulent in ppl, spread quickly (pandemic)

103
Q

Avian Influenza - Clinical Signs - general statement

A

-Infection may cause a wide range of clinical signs from no disease (asymptomatic), respiratory disease, to severe disease with high mortality
-localized infection - mild to moderate disease
~intestinal-wild ducks and shorebirds, poultry
~Respiratory- humans, swine, horses, poultry, domestic ducks, seal, mink
-Systemic infection-high mortality
~chickens, turkeys, other gallinaceous birds

104
Q

Avian Influenza - Clinical Signs

A

Sudden death with no clinical signs, lack of energy and appetite, decreased egg production, swelling of head, eyelids, combs, wattles, hocks; purple discoloration of wattles, combs, legs; stumbling or falling down; diarrhea

105
Q

Avian Influenza - Prevention (Steps 1 - 3)

A

1) Keep your distance
~restrict access to your property and your birds
2) Keep it clean
~wash hands, clothes, equipment before and after
3) Don’t haul disease home
~new birds and birds that have traveled to shows be quarantined prior to reintegration; buy from reputable sources

106
Q

Avian Influenza - Prevention (Steps 4 - 6)

A
  1. Don’t borrow disease from your neighbors
    ~do not borrow equipment/bird supply from other bird owners; if you do, disinfect before arriving at your property
  2. Know the warning signs
    ~check frequently; know if something is wrong early
  3. Report sick birds
    ~if your birds are sick or dying, calling state vet, USDA, etc.
107
Q

Avian Influenza - Control

A

1) Increased surveillance
2) Stamping Out (Disinfection and movement control)
3) Vaccination
4) Restructuring (compartmentalization)

108
Q

Bioterrorism - AI - Veterinarians’ preparedness responsibilities

A
  • Anticipate outbreaks on the local level
  • collect and label samples
  • know the agents
  • know the typical signs of diseases (animals and humans)
  • know how to report suspected cases
  • disseminate knowledge
109
Q

Public Health Security and Bioterrorism Preparedness Response Act of 2002

A
  • Improve ability of the US to prevent, prepare for, and respond to bioterrorism and other public health emergencies
  • $4.3 billion to various federal, state and local agencies
  • Five titles
110
Q

Public Health Security and Bioterrorism Preparedness Response Act of 2002 - 5 titles

A

1) National preparedness for bioterrorism and other public health emergencies
2) enhancing controls on dangerous biological agents and toxins
3) protecting safety and security of food and drug supply
4) drinking water security and safety
5) Additional provisions

111
Q

Department of homeland security (DHS)

A
  • established January 2003
  • Mission: Prevent, protect, and respond to acts of terrorism on US soil
  • 4 policy directorates
112
Q

DHS’s four policy directorates

A

1) Guard borders and airports
2) coordinate the response for future emergencies
3) analyze threats and intelligence
4) protect our critical infrastructure

*Responsibilities for coordinating HHS and USDA

113
Q

Centers for Disease Control and Prevention - Mission

A

Mission: Promote health and quality of life by preventing and controlling disease, injury, and disability

  • preparing for bioterrorism since 1998
  • one of the first agencies to respond to anthrax incidents of 2001
114
Q

strategic national stockpile

A

-12 hour push package
~complete package of medical materials
-vendor managed inventory
~tailored to suspected agents

115
Q

CDC classification of bioterrorism agents - general criteria

A

1) The public health impact based on illness and death
2) the delivery potential to large populations based on stability and ability to mass produce and distribute a virulent agent
3) potential for person to person transmission
4) the public perception as related to public fear and potential civil disruption
5) special public health preparedness needs, stockpiled required, surveillance and diagnostic needs

116
Q

CDC classification - general statement

A

Special attention was given to those agents that had previously been used or researched as a bioweapon. Based on these criteria, agents were scored and divided into A, B, and C Categories. This is not a federally legislated list and is subject to change based on review of agents. Using this standardized system allows the CDC to add or remove agents

117
Q

Weaponization of Agents

A
  • *Alter characteristics of a pathogen to make it a more effective weapon:
    1) enhance transmission
    2) Increase virulence
    3) Resistant to antibiotics
    4) Evade vaccine protection
    5) Alter clinical signs
118
Q

CDC’s Category A Bioterrorism Agents - requirements

A

High-priority agents include organisms that pose a risk to national security because they:

1) can be easily disseminated or transmitted from person to person
2) result in high mortality rates and have the potential for major public health impact
3) might cause public panic and social disruption
4) require special action for public health preparedness

119
Q

CDC’s Category A Bioterrorism Agents/Diseases

A

1) Anthrax (Bacillus anthracis)
2) Botulism (Clostridium botulinum toxin)
3) Plague (Yersinia Pestis)
4) Smallpox (variola major)
5) Tularemia (Francisella tularensis)
6) Viral hemorrhagic fevers (filoviruses [e.g. Ebola, Marburg] and arenaviruses [e.g. Lassa, Machupo])

120
Q

CDC’s Category B Bioterrorism Agents - Requirements

A

Second highest priority agents include those that:

1) are moderately easy to disseminate
2) result in moderate morbidity rates and low mortality rates;
3) require specific enhancements of CDC’s diagnostic capacity and enhanced disease surveillance

121
Q

CDC’s Category B Bioterrorism Agents/Diseases

A

1) Brucellosis (Brucella species)
2) Epsilon toxin of Clostridium perfringens
3) Food safety threats (e.g. Salmonella species, Escherichia coli 0157:H7; Shigella)
4) Glanders (Burkholderia mallei)
5) Melioidosis (Burkholderia pseudomallei)
6) Psittacosis (Chlamydia pisttaci
7) Q Fever (coxiella burnetii)
8) Ricin toxin from Ricinus communis (castor beans)
9) Staphylococcal enterotoxin B
10) Typhus fever (Rickettsia prowazekii)
11) Viral encephalitis (alphaviruses [e.g. Venezuelan equine encephalitis, eastern equine encephalitis, western equine encephalitis])
12) Water safety threats (e.g. vibrio cholerae, cryptosporidium parvum)

122
Q

CDC’s Category C Bioterrorism Agents - Requirements

A

Third highest priority agents include emerging pathogens that could be engineered for mass dissemination in the future because of:

1) availability
2) ease of production and dissemination
3) potential for high morbidity and mortality rates and major health impacts

123
Q

CDC’s Category C Bioterrorism Agents/Diseases

A

Emerging infectious diseases such as Nipah virus and Hantavirus

124
Q

Federal Select Agent Program - major players

A 
Jointly comprised of:
CDC
Division of select agents and toxins
Animal and Plant Health Inspection services
Agriculture Select Agent services
125
Q

Federal Select Agent Program - what it does

A

oversees the possession, use and transfer of biological select agents and toxins, which have the potential to pose a severe threat to public, animal or plant health or to animal or plant products

Foreign Animal Diseases (2 decks)

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